The Plant Mind: Unraveling Abiotic Stress Priming, Memory, and Adaptation

Abstract

Plants exhibit a remarkable capacity to adapt to recurrent abiotic stresses, prompting a re-evaluation of traditional views on plant responses to environmental challenges. This review explores the intricate mechanisms of stress priming, memory, and adaptation in plants. Specifically, it details the molecular and physiological processes underlying abiotic stress priming, which serve as a gateway to understanding plant memory. Stress priming fosters resilience against diverse stressors through interconnected pathways involving hormone signaling, transcriptional regulation, DNA methylation, histone modifications, and small RNAs. These epigenetic changes orchestrate stress-responsive gene expression and can, in some cases, be passed on to future generations. This review distinguishes between somatic memory, intergenerational effects, and transgenerational inheritance to avoid conceptual overlap. By connecting short-term priming to long-term adaptation and potential heritability, this article proposes a paradigm shift in how plant resilience is understood, with significant implications for crop improvement under climate stress.

Keywords: adaptation; climate change; epigenetic modifications; stress memory; transgenerational inheritance.

FIGURE 1

Plant responses to abiotic stress involving perception, biochemical signaling, and epigenetic regulation underlying stress priming, memory formation, and adaptive resilience to recurrent environmental challenges. (A) Stress stimuli trigger secondary messengers (Ca²⁺, ROS, cAMP), activating pathways like MAPK and CDPK, which induce histone modifications and transcription of stress‐responsive genes (e.g., WRKY, MYB, NAC), leading to stress memory formation and adaptation. (B) Initial stress exposure helps establish stress memory, enabling faster and stronger responses to recurrent or secondary stress events. (C) Primed plants show improved ROS regulation and stress tolerance upon secondary stress, unlike unprimed plants, which remain stress‐sensitive. (D) Stress priming leads to memory gene activation, enabling short‐term and transgenerational memory. Epigenetic regulation supports memory acquisition, while resetting ensures adaptability to future stress.

FIGURE 2

Stress imprint formation and cross‐talk signaling between various stresses. Stresses stimulate the synthesis of endogenous signaling molecules such as hydrogen peroxide (H₂O₂), nitric oxide (NO), calcium ions (Ca²⁺), inositol‐1,4,5 trisphosphate (IP3), kinases, and phytohormones. These compounds regulate downstream signal cascades and induce cross‐tolerance against a plethora of stresses by modulating phytohormone signaling, synthesizing compatible solutes to maintain osmotic balance such as sugars, amino acids, and glycine betaines, enhancing antioxidant activities (such as SOD, CAT, and APX), activating proteins that help cope with stress, for example, HSP, dehydrins, and LEA, triggering the expression of stress‐responsive genes (such as NAC, DREB, MYB, MYC, and WRKY), and causing epigenetic changes.

FIGURE 3

Illustration of the process of transgenerational stress priming and memory imprinting in plants. The F1 generation inherits stress memory from the parental generation, allowing them to adapt to harsh environments through transgenerational stress memory.

FIGURE 4

Mechanism of stress‐induced epigenetic memory formation via the RNA interference pathway in plants. Abiotic stress triggers the production of double‐stranded RNA (dsRNA), which is processed by Dicer into small interfering RNAs (siRNAs). These siRNAs are loaded onto Argonaute proteins, guiding the recruitment of DNA methyltransferases and histone modifiers to specific genomic loci. This leads to the establishment of stress‐specific epigenetic marks, such as DNA methylation and histone modifications, ultimately contributing to stable transgenerational inheritance of stress memory.